Fig. 3

A quaternary YAP–TEAD2/β-catenin-TCF complex is essential for maintaining expression of Oct4. a YAP ChIP-seq in zsRASSF1A-overexpressing versus control ESC depicting reduced occupancy of YAP–TEAD and YAP-β-catenin target genes in the presence of RASSF1A. See also Supplementary Fig. 3a, b, 4 and Data 6. b Enriched sequence motifs (P < 0.05) identified in the proximity of upregulated YAP target genes upon RASSF1A loss in ESC. See also Supplementary Data 2. c YAP, TEAD2 and β-catenin ChIP on TEAD2 and TCF binding sites (BS) on the ESC Pou5f1/Oct4 promoter in response to indicated conditions. d Proteomics analysis for YAP binding partners in empty vector versus zsRASSF1A-transfected ESC. Factors modifying their affinity with YAP are represented by relative abundance of peptides (LFQ intensity) and fold difference to maximum. All mass-spec intensities were normalised to YAP intensities. See also Supplementary Fig. 3c and Data 3. e Size exclusion chromatography of ESC lysates via Gel filtration column and western blotting with indicated antibodies. See also Supplementary Fig. 3d. f Western blotting of YAP and TEAD2 immunoprecipitates in response to transient depletion of RASSF1A. Validation using #2 siRassf1A and shRassf1A is provided in Supplementary Fig. 3e–g. g YAP ChIP at TEAD and β-catenin/TCF binding sites (BS) on the ESC Pou5f1/Oct4 promoter in response to stable ablation of RASSF1A versus control. *P < 0.05, **P < 0.01 and ***P < 0.001, respectively, of Student’s t-test. Error bars indicate s.e.m. Data shown are representative of at least three independent experiments